急性痛风性关节炎可造成关节部位剧痛，患者疼痛难耐，严重影响生活质量，而抗痛风药副作用明显。针刺在临床上可有效缓解急性痛风性关节炎疼痛，且无明显副作用，但其镇痛机制尚未明确。前期研究中，申请人利用RNA-Seq技术发现IL-33/ST2通路在小鼠痛风关节表达增高，且敲除ST2可缓解痛风小鼠痛行为。申请人近期一项研究发现IL-33/ST2通路在介导外周感觉神经元兴奋性方面有重要作用。本项目拟在前期研究基础上，以IL-33/ST2通路激动感觉神经元和引发炎症部位中性粒细胞浸润为切入点，整合免疫学、细胞内钙成像、膜片钳、逆行标记、行为学和转基因动物等手段，探讨该通路参与急性痛风性关节炎疼痛的神经免疫机制，并探讨电针对该通路的干预作用。该研究将揭示急性痛风性关节炎疼痛产生的崭新机制，并为针刺治疗急性痛风性关节炎提供重要理论依据，有助于推动其作为“绿色疗法”用于急性痛风性关节炎疼痛的临床治疗。

Acute gout arthritis (AGA) can induce severe pain in the joint and surrounding tissues, which usually makes the patient hard to endure and severely affects his/her life quality. Acupuncture effectively alleviates AGA pain in clinic, while exerting no obvious side effects. However, the mechanisms underlying its analgesic effect on AGA-induced pain is not fully understood yet. In our previous studies, we identified that the expression of IL-33/ST2 signaling pathway is significantly up-regulated in the gouty joints of mice by means of RNA-Seq technique. In addition, ST2 knockout significantly reduced the nocifensive behaviors of AGA model mice. Our recent study demonstrated that IL-33/ST2 pathway plays a pivotal role in mediating peripheral sensory neuron excitability. Therefore, this project aims to investigate IL-33/ST2-induced sensory neuron excitability and IL-33/ST2-induced neutrophil infiltration in inflammatory joints by means of immune blot/fluorescence, calcium imaging, patch clamp, retrograde labeling, behavioral assay and transgenic mice, etc., all of which will help to reveal the neuroimmune mechanisms of IL-33/ST2 pathway involved in AGA pain. Next,the project aims to explore the interventions of electroacupuncture on IL-33/ST2 pathway. In all, this project will unravel the novel molecular mechanisms involved in AGA-induced pain and provide important theory to support the treatment of AGA with acupuncture. This project may help to further promote the clinical practice of acupuncture in treating AGA-induced pain as a “green therapy”.